The DOI matches its Crossref record.
Role of LXR and ABCA1 in the Pathogenesis of Alzheimers Disease -Implications for a New Therapeutic Approach
Abstract
Studies, ranging from epidemiological to in vitro and in vivo experimental settings have provided convincing evidence that different aspects of brain lipid metabolism may influence Alzheimer disease pathogenesis through effects on beta-amyloid deposition and clearance. It has been demonstrated that transcription factors called nuclear liver X receptors (LXR) and their responsive genes provide natural regulatory mechanisms and influence AD pathogenesis through their modulatory effects on intracellular cholesterol content, cholesterol efflux and possibly via anti-inflammatory mechanisms. Here, we provide a brief summary of the approaches undertaken by different groups that lead to the nowadays working model of LXR and ABCA1 regulatory role in brain amyloidogenesis and amyloid clearance and we highlight the therapeutic potential of LXR agonists.
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Bexarotene might upregulate ABCB1 expression via the formation of RXR/LXR heterodimers.
“Therefore, bexarotene might upregulate ABCB1 expression via the formation of RXR/LXR heterodimers; this would be a very attractive therapeutic approach for AD [72].”
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Overexpression of ABCA1 reduces amyloid deposition in the PDAPP mouse model of Alzheimer disease
Wahrle, S. E., Jiang, H., Parsadanian, M., Kim, J., Li, A., Knoten, A., Jain, S., Hirsch-Reinshagen, V., Wellington, C. L., Bales, K. R., et al. (2008) · Journal of Clinical Investigation · doi:10.1172/jci33622 · Cited by 370
Metabolic Network Analysis Reveals Altered Bile Acid Synthesis and Metabolism in Alzheimer’s Disease
Baloni, P., Funk, C. C., Yan, J., Yurkovich, J. T., Kueider-Paisley, A., Nho, K., Heinken, A., Jia, W., Mahmoudiandehkordi, S., Louie, G., et al. (2020) · Cell Reports Medicine · doi:10.1016/j.xcrm.2020.100138 · Cited by 211
ApoE Lipidation as a therapeutic target in Alzheimer’s disease
Lanfranco, M. F., Ng, C. A., & Rebeck, G. W. (2020) · International Journal of Molecular Sciences · doi:10.3390/ijms21176336 · Cited by 189
miR-106b impairs cholesterol efflux and increases Aβ levels by repressing ABCA1 expression
Kim, J., Yoon, H., Ramírez, C. M., Lee, S.-M., Hoe, H.-S., Fernández-Hernando, C., & Kim, J. (2012) · Experimental Neurology · doi:10.1016/j.expneurol.2011.11.010 · Cited by 173
“…is sufficient to impair cellular cholesterol efflux. miR-106b increases levels of secreted Aβ Previous in vitro and in vivo studies demonstrated that ABCA1 influences Aβ levels (Bu, 2009; Fan et al., 2009; Hirsch-Reinshagen and Wellington, 2007; Kim et al., 2009; Koldamova and Lefterov, 2007).”
BackgroundResultFitz, N. F., Cronican, A. A., Lefterov, I., & Koldamova, R. (2013) · Science · doi:10.1126/science.1235809 · Cited by 151
Self-citationLefterov, I., Bookout, A., Wang, Z., Staufenbiel, M., Mangelsdorf, D., & Koldamova, R. (2007) · Molecular Neurodegeneration · doi:10.1186/1750-1326-2-20 · Cited by 89
Self-citationKuntz, M., Candela, P., Saint-Pol, J., Lamartinière, Y., Boucau, M.-C., Sevin, E., Fenart, L., & Gosselet, F. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-150469 · Cited by 55
Li, G., Kim, C., Kim, J., Yoon, H., Zhou, H., & Kim, J. (2015) · Journal of Alzheimer's Disease · doi:10.3233/jad-150024 · Cited by 39
Metadata
- Authors
- Koldamova, R., & Lefterov, I.
- Venue
- Current Alzheimer Research
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2007-04-01
- Volume
- 4
- Issue
- 2
- Pages
- 171-178
- ISSN
- 1567-2050
- Cited by
- 56
- References
- 0
- Language
- en
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